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Molecular Biology of the Pituitary 2.0
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Molecular Biology of the Pituitary 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 14474

Special Issue Editors

Prof. Dr. Salvatore Maria Corsello

E-Mail Website
Guest Editor
Department of Translational Medicine and Surgery, Unit of Endocrinology, Università Cattolica del Sacro Cuore—Fondazione Policlinico “Gemelli” IRCCS, Largo Gemelli 8, I-00168 Rome, Italy
Interests: pituitary; acromegaly; Cushing’s syndrome; hyperprolactinemia; TSH-secreting pituitary adenoma; syndrome of reduced sensitivity to thyroid hormones; thyroid; adrenal gland
Special Issues, Collections and Topics in MDPI journals
Dr. Rosa Maria Paragliola

E-Mail Website
Guest Editor
Department of Translational Medicine and Surgery, Unit of Endocrinology, Università Cattolica del Sacro Cuore—Fondazione Policlinico “Gemelli” IRCCS, Largo Gemelli 8, I-00168 Rome, Italy
Interests: pituitary; acromegaly; Cushing’s syndrome; hyperprolactinemia; TSH-secreting pituitary adenoma; syndrome of reduced sensitivity to thyroid hormones; thyroid; adrenal gland
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to present recent research on the molecular biology of pituitary diseases. Pituitary adenoma is a common disease, present in about 10% of the general population, which generally presents as benign tumors. However, rarely, tumors can become malignant and metastasize. Pituitary adenomas are also associated with specific syndromes (e.g., acromegaly, Cushing’s syndrome, prolactinoma, inappropriate TSH secretion syndrome) due to inappropriate hormonal secretion. The continuous development of molecular biology techniques has improved the understanding of both the pathogenesis and the biology of these tumors and this knowledge can be applied for the development of diagnostic approaches and therapeutic options. Interestingly, molecular biology techniques have led to the discovery of the pathophysiological mechanisms at the basis of non-neoplastic pituitary diseases, such as thyroid hormone resistance syndrome or non-neoplastic TSH inappropriate secretion. Regarding syndromes of reduced sensitivity to thyroid hormones, an important topic is the discovery of polymorphisms in genes which code for type 2 deiodinase. Finally, genetic analyses can identify mutations of genes coding for transcription factors involved in pituitary development, which can be involved in the pathogenesis of combined pituitary hormone deficiency.

Prof. Dr. Salvatore M. Corsello
Dr. Rosa Maria Paragliola
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • acromegaly
  • somatostatin receptor ligands
  • prolactinoma
  • Cushing’s syndrome
  • TSH-secreting adenomas
  • syndromes of reduced sensitivity to thyroid hormones
  • pituitary adenomas
  • pituitary carcinomas
  • hypopituitarism

Published Papers (5 papers)

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Research

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16 pages, 1767 KiB  
Article
Difference in miRNA Expression in Functioning and Silent Corticotroph Pituitary Adenomas Indicates the Role of miRNA in the Regulation of Corticosteroid Receptors
by Beata J. Mossakowska, Paulina Kober, Natalia Rusetska, Joanna Boresowicz, Maria Maksymowicz, Monika Pękul, Grzegorz Zieliński, Andrzej Styk, Jacek Kunicki, Tomasz Mandat and Mateusz Bujko
Int. J. Mol. Sci. 2022, 23(5), 2867; https://doi.org/10.3390/ijms23052867 - 5 Mar 2022
Cited by 6 | Viewed by 2356
Abstract
Corticotroph pituitary adenomas commonly cause Cushing’s disease (CD), but some of them are clinically silent. The reason why they do not cause endocrinological symptoms remains unclear. We used data from small RNA sequencing in adenomas causing CD (n = 28) and silent [...] Read more.
Corticotroph pituitary adenomas commonly cause Cushing’s disease (CD), but some of them are clinically silent. The reason why they do not cause endocrinological symptoms remains unclear. We used data from small RNA sequencing in adenomas causing CD (n = 28) and silent ones (n = 20) to explore the role of miRNA in hormone secretion and clinical status of the tumors. By comparing miRNA profiles, we identified 19 miRNAs differentially expressed in clinically functioning and silent corticotroph adenomas. The analysis of their putative target genes indicates a role of miRNAs in regulation of the corticosteroid receptors expression. Adenomas causing CD have higher expression of hsa-miR-124-3p and hsa-miR-135-5p and lower expression of their target genes NR3C1 and NR3C2. The role of hsa-miR-124-3p in the regulation of NR3C1 was further validated in vitro using AtT-20/D16v-F2 cells. The cells transfected with miR-124-3p mimics showed lower levels of glucocorticoid receptor expression than control cells while the interaction between miR-124-3p and NR3C1 3′ UTR was confirmed using luciferase reporter assay. The results indicate a relatively small difference in miRNA expression between clinically functioning and silent corticotroph pituitary adenomas. High expression of hsa-miR-124-3p in adenomas causing CD plays a role in the regulation of glucocorticoid receptor level and probably in reducing the effect of negative feedback mediated by corticosteroids. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary 2.0)
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Review

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17 pages, 934 KiB  
Review
Genetic Basis of ACTH-Secreting Adenomas
by Pietro Locantore, Rosa Maria Paragliola, Gianluca Cera, Roberto Novizio, Ettore Maggio, Vittoria Ramunno, Andrea Corsello and Salvatore Maria Corsello
Int. J. Mol. Sci. 2022, 23(12), 6824; https://doi.org/10.3390/ijms23126824 - 19 Jun 2022
Cited by 1 | Viewed by 1895
Abstract
Cushing’s disease represents 60–70% of all cases of Cushing’s syndrome, presenting with a constellation of clinical features associated with sustained hypercortisolism. Molecular alterations in corticotrope cells lead to the formation of ACTH-secreting adenomas, with subsequent excessive production of endogenous glucocorticoids. In the last [...] Read more.
Cushing’s disease represents 60–70% of all cases of Cushing’s syndrome, presenting with a constellation of clinical features associated with sustained hypercortisolism. Molecular alterations in corticotrope cells lead to the formation of ACTH-secreting adenomas, with subsequent excessive production of endogenous glucocorticoids. In the last few years, many authors have contributed to analyzing the etiopathogenesis and pathophysiology of corticotrope adenomas, which still need to be fully clarified. New molecular modifications such as somatic mutations of USP8 and other genes have been identified, and several case series and case reports have been published, highlighting new molecular alterations that need to be explored. To investigate the current knowledge of the genetics of ACTH-secreting adenomas, we performed a bibliographic search of the recent scientific literature to identify all pertinent articles. This review presents the most recent updates on somatic and germline mutations underlying Cushing’s disease. The prognostic implications of these mutations, in terms of clinical outcomes and therapeutic scenarios, are still debated. Further research is needed to define the clinical features associated with the different genotypes and potential pharmacological targets. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary 2.0)
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14 pages, 1908 KiB  
Review
The Role of Glucocorticoid Receptor in the Pathophysiology of Pituitary Corticotroph Adenomas
by Daniela Regazzo, Alessandro Mondin, Carla Scaroni, Gianluca Occhi and Mattia Barbot
Int. J. Mol. Sci. 2022, 23(12), 6469; https://doi.org/10.3390/ijms23126469 - 9 Jun 2022
Cited by 2 | Viewed by 2320
Abstract
Adrenocorticotropic Hormone (ACTH)-secreting pituitary adenomas are rare tumors characterized by autonomous ACTH secretion with a consequent increase in circulating cortisol levels. The resulting clinical picture is called Cushing’s disease (CD), a severe condition burdened with high morbidity and mortality. Apart from increased cortisol [...] Read more.
Adrenocorticotropic Hormone (ACTH)-secreting pituitary adenomas are rare tumors characterized by autonomous ACTH secretion with a consequent increase in circulating cortisol levels. The resulting clinical picture is called Cushing’s disease (CD), a severe condition burdened with high morbidity and mortality. Apart from increased cortisol levels, CD patients exhibit a partial resistance to the negative glucocorticoid (GC) feedback, which is of paramount clinical utility, as the lack of suppression after dexamethasone administration is one of the mainstays for the differential diagnosis of CD. Since the glucocorticoid receptor (GR) is the main regulator of negative feedback of the hypothalamic–pituitary–adrenal axis in normal conditions, its implication in the pathophysiology of ACTH-secreting pituitary tumors is highly plausible. In this paper, we review GR function and structure and the mechanisms of GC resistance in ACTH-secreting pituitary tumors and assess the effects of the available medical therapies targeting GR on tumor growth. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary 2.0)
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20 pages, 380 KiB  
Review
Effects of Pituitary Adenylate Cyclase Activating Polypeptide on Cell Death
by Gabriella Horvath, Dora Reglodi, Eszter Fabian and Balazs Opper
Int. J. Mol. Sci. 2022, 23(9), 4953; https://doi.org/10.3390/ijms23094953 - 29 Apr 2022
Cited by 4 | Viewed by 1596
Abstract
Pituitary adenylate cyclase activating polypeptide (PACAP) was first isolated as a hypothalamic peptide based on its efficacy to increase adenylate cyclase (AC) activity. It has a widespread distribution throughout the body including the nervous system and peripheral organs, where PACAP exerts protective effects [...] Read more.
Pituitary adenylate cyclase activating polypeptide (PACAP) was first isolated as a hypothalamic peptide based on its efficacy to increase adenylate cyclase (AC) activity. It has a widespread distribution throughout the body including the nervous system and peripheral organs, where PACAP exerts protective effects both in vivo and in vitro through its anti-apoptotic, anti-inflammatory, and antioxidant functions. The aim of the present paper was to review the currently available literature regarding the effects of PACAP on cell death in vitro in neural and non-neural cells. Among others, its effect on apoptosis can be detected in cerebellar granule cells against different toxic stimuli. Different neural cell types from the cerebral cortex are also prevented from cell death. PACAP also shows effects on cell death in cells belonging to the peripheral nervous system and protects both neural and non-neural cells of sensory organs. In addition, cell survival-promoting effect can be observed in different peripheral organ systems including cardiovascular, immune, respiratory, gastrointestinal, urinary, and reproductive systems. The studies summarized here indicate its noteworthy effect on cell death in different in vitro models, suggesting PACAP’s potential therapeutic usage in several pathological conditions. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary 2.0)
15 pages, 1564 KiB  
Review
Molecular Pathways in Prolactinomas: Translational and Therapeutic Implications
by Betina Biagetti and Rafael Simò
Int. J. Mol. Sci. 2021, 22(20), 11247; https://doi.org/10.3390/ijms222011247 - 18 Oct 2021
Cited by 5 | Viewed by 5441
Abstract
Prolactinoma has the highest incidence rate among patients with functional pituitary tumours. Although mostly benign, there is a subgroup that can be aggressive. Some clinical, radiological and pathology features have been associated with a poor prognostic. Therefore, it can be considered as a [...] Read more.
Prolactinoma has the highest incidence rate among patients with functional pituitary tumours. Although mostly benign, there is a subgroup that can be aggressive. Some clinical, radiological and pathology features have been associated with a poor prognostic. Therefore, it can be considered as a group of heterogeneous tumours. The aim of this paper is to give an overview of the molecular pathways involved in the behaviour of prolactinoma in order to improve our approach and gain deeper insight into the better understanding of tumour development and its management. This is essential for identifying patients harbouring aggressive prolactinoma and to establish personalised therapeutics options. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary 2.0)
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